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MSK II Exam I > Intro to pharm > Flashcards

Intro to pharm Flashcards

1
Q

Antibacterial Agents

A

Bacitracin and gramicidin
Mupirocin
Polymyxin B sulfate
Neomycin and gentamicin

Topical antibiotics in acne: 
Clindamycin (Cleocin)  
Erythromycin (Erygel)
Metronidazole (Metrogel)
Sodium sulfacetamide
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2
Q

Topical Antiviral Agents

A

Acyclovir, penciclovir, docosanol (Abreva)

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3
Q

Topical antifungal preparations

A 
Azoles – clotrimazole
miconazole 
ketoconazole, 
Ciclopirox olamine 
Allylamines – terbinafine 
Butenafine
Tolnaftate 
Nystatin and amphotericin B
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4
Q

Oral antifungal agents

A

Azoles – ketoconazole, itraconazole, fluconazole, voriconazole

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5
Q

Immunomodulators

A

Imiquimod

Tacrolimus and pimecrolimus

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6
Q

Acne Preparations

A

Retinoic acid and derivatives: retinoic acid (tretinoin), adapalene ,
tazarotene
Isotretinoin
Benzoyl peroxide

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7
Q

Drugs for Psoriasis

A

Acitretin
Tazarotene
Calcipotriene
Cyclosporine

Biologic response modifiers
TNF inhibitors – etanercept
infliximab , adalimumab

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8
Q

Anti-Inflammatory Agents

A

Topical corticosteroids

Examples include hydrocortisone, hydrocortisone valerate, triamcinolone acetonide, betamethasone

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9
Q

Keratolytic and Destructive Agents

A

Salicylic acid

Fluorouracil

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10
Q

Antipruritic Agents

A

Antihistamines

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11
Q

Trichogenic and Antitrichogenic Agents

A

Minoxidil , finasteride

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12
Q

Skin function:

A 
Protection
Thermal regulation
Immune responsiveness
Biochemical synthesis
Sensory detection
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13
Q

Variables determining response

A

Drug penetration
Concentration gradient
Dosing schedule
Vehicles and occlusion

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14
Q

Drug Absorption

A

Three routes:

  • Intact stratum corneum
  • Sweat ducts
  • Sebaceous follicles

Steps involved in percutaneous absorption:

  • Concentration gradient established
  • Partition coefficient
  • Diffusion coefficient

Rate of absorption:
J = Cveh · Km · D/x

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15
Q

drying preparations to lubricating preparations

A

tinctures < wet dressings < lotions < gels < aerosols < powders < pastes < creams < ointments

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16
Q

what do we use for Chronic inflammation with xerosis, scaling, lichenification

A

creams and ointments

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17
Q

what do we use for Acute inflammation with oozing, vesiculation, and crusting

A

tinctures, wet dressings, and lotions

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18
Q

Transdermal Patches

A 
fentanyl for pain
lidocaine for neuralgia 
ethinyl estradiol/ norelgestromin for contraception
nitroglycerin for angina
scopolaine for motion sickness
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19
Q

general treatment approach for abrasions

A

clean minor injuries (scratches, cuts, abrasions) with soap and water
use of topical abx is mixed– worry about skin sensitivity/ promotion of resistance
clean wounds and remove debris

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20
Q

What are the mechanisms of action of the individual components of Neosporin (bacitracin, neomycin, polymyxin B)?

A. Increases permeability of cell wall
B. Inhibits cell wall synthesis
C. Inhibits 30S ribosomal subunit

A

polymixin B- increases permeability of cell wall
bacitracin- inhibits cell wall synthesis
neomycin- inhibits 30S ribosomal subunit

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21
Q

A 5 yo female is brought to urgent care by her mother after returning from kindergarten with red sores around her mouth.
You suspect non-bullous impetigo and would like to suggest a topical antibiotic ointment.
Which two topical antimicrobials cover group A β-hemolytic streptococci and S. aureus (including MRSA)?
Mupirocin
Neomycin
Polymyxin B
Retapamulin

A

neomycin and polymyxin B are not good for gram positive organisms.

Use mupirocin and retapamulin

mupirocin has good in vitro activity against MRSA but there’s no good clinical evidence

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22
Q

kid with non-bullous impetigo. General treatment approach

A

non-bullous impetigo- topical therapy with mupirocin or retapamulin for 5 days

more extensive forms of impetigo and bullous forms- oral abx for 7 days

Benefits of topical therapy: fewer side effects, lower risk of bacterial resistance.

Bacitracin-neomycin-polymixin B has some activity against impetigo causing organisms, but- may be less effective, and bacitracin and neomycin can cause contact dermatitis

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23
Q

Topical Antibiotics in Acne

A

Avoid systemic exposure and achieve high follicular concentrations
Less effective than systemic administration of the same antibiotic
Available options:
- Clindamycin
- Erythromycin
- Metronidazole
- Sodium sulfacetamide

Not used as monotherapy (bacterial resistance)!
- Give with benzoyl peroxide or retinoids

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24
Q

Clindamycin MOA

A

inhibits 50s ribosomal subunit

25
Q

erythromycin MOA

A

inhibits 50s ribosomal subunnit

26
Q

metronidazole MOA

A

damages DNA

27
Q

sodium sulfacetamide MOA

A

inhibits folic acid synthesis

28
Q

increased sebum production in acne creates a lipi rich microaerobic environment favorable to what organism?

A

propionibacterium acnes

29
Q

A 35 yo male construction worker presents to his PCP with complaints of intense itching of both feet throughout the day.
PE: webs spaces white, macerated, cracked
Workup consistent with dermatophyte infection
What topical therapeutic options are available?

A

azoles, allylamine, butenafine, tolnaftate

pt/ provider preference, etc.

30
Q

topical Azoles – clotrimazole, miconazole

MOA, uses

A

MOA: inhibits synthesis of ergosterol (inhibits lanosterol 14-α-demethylase)
Uses: tinea corporis (ring worm), tinea pedis (athlete’s foot), tinea cruris (jock itch), tinea versicolor, and cutaneous candidiasis, such as vaginal yeast infections, infections of the skin, diaper rash, and thrush (candidiasis of the oral mucosa and tongue, and sometimes the palate, gingivae, and floor of the mouth)

31
Q

topical Ciclopirox olamine

MOA, uses

A

MOA: inhibits uptake of precursors of macromolecule synthesis
Uses: topical dermatomycosis, candidiasis, tinea versicolor, mild-to-moderate onychomycosis

32
Q

topical Allylamines – terbinafine and naftifine

MOA, uses

A

MOA: inhibits squalene epoxidase
Uses: tinea corporis, tinea cruris, and tinea pedis

33
Q

topical tolnaftate MOA, uses

A

MOA unknown.

Uses: tinea pedis, tinea cruris, and tinea corporis

34
Q

topical
Nystatin/amphotericin B
MOA, uses

A

MOA: binds ergosterol in fungal cell membrane altering permeability
Nystatin limited to topical cutaneous and mucosal uses
- Thrush
Amphotericin B broad antifungal spectrum but rarely used topically
Cumulative organ toxicity “ampho-terrible”

35
Q

oral azoles: uses

A

Uses: vaginal, urinary, oropharyngeal, or esophageal candida infections
Systemic yeast infections more common: type 1 diabetes, leukemia, AIDS
Drug-drug interactions!

36
Q

oral griseofulvin: MOA, uses

A

MOA: inhibits fungal cell mitosis at metaphase
Uses: dermatophyte infections but not Candida
Induces CYP enzymes

37
Q

oral terbinafine: uses

A

High first pass metabolism; accumulates in skin, nails, fat

Uses: tinea corporis, tinea capitis, and onychomycosis

38
Q

Antifungal Agents for dermatophyte infections- by location

A 
Tinea capitis (scalp) – oral griseofulvin, terbinafine, itraconazole
Tinea pedis (feet) – topical antifungals
Tinea cruris (groin) – topical antifungals
Tinea corporis (body) – topical antifungals, oral antifungals
39
Q

antifungal agents for candida

A

Thrush (oropharyngeal candidiasis) – oral nystatin, clotrimazole troche, oral fluconazole
Esophageal candidiasis – systemic antifungals
Vulvovaginitis – topical antifungals, oral fluconazole
Invasive infection – systemic antifungals

40
Q

A 40 yo male seeks your recommendation regarding frequent cold sores.
He experiences about ten cold sores a year, exacerbated by “colds” or sun exposure.
What organism is causing these cold sores?

He wants to know what treatment options are available to him.

A

Herpes simplex

topical acyclovir, penciclovir, or docosonol- modest benefit
apply within 1 hour of first sign or symptom, continue x 4 days

oral acyclovir, famcyclovir, valacyclovir- begin within 1 hour

chronic suppressive therapy for > 6 recurrences per year (acyclovir, valacyclovir)

41
Q

Acyclovir, valacyclovir, penciclovir, famciclovir

MOA, uses

A

MOA: converted to pharmacologically active triphosphate metabolites, inhibit DNA synthesis and viral replication
Topical – modest benefit for herpes labialis
Systemic –
Most effective in treating herpes labialis
Also used systemically for HSV and VZV infections

42
Q

Docosanol

MOA and uses

A

MOA: inhibits fusion between the plasma membrane and the HSV envelope, thereby preventing viral entry and replication
When applied within 12 hours of the onset of prodromal symptoms, five times daily, median healing time was shortened by 18 hours compared with placebo in recurrent orolabial herpes

43
Q

Imiquimod

MOA, uses, ADRs

A

MOA: may be related to stimulation of peripheral mononuclear cells to release interferon-α and macrophage stimulation to produce interleukins-1, -6, -8, and TNF-α
Uses: external genital and perianal warts in adults, actinic keratoses on the face and scalp, biopsy-proven primary basal cell carcinomas on the trunk, neck, and extremities (< 2 cm diameter)
ADRs: local inflammation, pruritus, erythema, superficial erosion

44
Q

Tacrolimus

MOA, uses, ADRs

A

MOA: inhibit T-lymphocyte activation and prevent release of inflammatory cytokines and mediators from mast cells
Uses: treatment of atopic dermatitis and psoriasis but traditionally used to prevent heart, liver, and kidney allograft rejection due to potent immunosuppressive activity (oral forms)
Topical ADRs: transient erythema, burning, and pruritus

45
Q

What is the mechanism of action of benzoyl peroxide?

A

releases free-radical oxygen which oxidizes bacterial proteins, activity against P. acnes (no resistance)

46
Q

14 y/o with mild acne. Other treatment options besides benzoyl peroxide?

A

topical retinoids: tretinoin (all-trans-retinoic acid)- also marketed as anti-aging
adapalene- photo-chemically more stable, less irritating
tazarotene– also approved for psoriasis, photoaging

MOA- may decrease cohesion between epidermal cells and increase epidermal cell turnover, expulsion of open comedones adn the transformation of closed comedones into open
ADRs: erythema, mild peeling and dryness; minimize sun exposure
CI: not recommended in pregnant women

47
Q

Severe Cystic Acne- treatment

A

Isotretinoin (PO)
MOA: reduces sebacerous gland size, reduces sebum production
PK: t1/2 10-20 hours; hepatic metabolism; highly protein bound (99-100%)
ADRs: resemble hypervitaminosis A (dryness and itching)

Must pledge to be on 2 contraceptives and take pregnancy tests

48
Q

Acne Treatment Approach

A

Comedonal (non-inflammatory) acne

  • Topical retinoid
    • Alternatives: azelaic acid, salicylic acid

Mild papulopustular and mixed acne
- Topical retinoid AND topical antimicrobial (BPO alone or BPO +/- topical antibiotic)

Moderate papulopustular and mixed acne
- Topical retinoid AND oral antibiotic AND topical BPO

Moderate nodular acne
- Topical retinoid AND oral antibiotic AND topical BPO

Severe nodular/conglobate acne
- Oral isotretinoin

49
Q

Psoriasis topical therapy

A

Emollients – used as basic adjunct; reduces scaling, itching, and related discomfort
Keratolytics – reduce hyperkeratosis; enable other topical drugs to penetrate
Topical glucocorticoids – rapid response; control inflammation and itching; mainstay of topical treatment

2nd line alternatives:

Coal tar
Anthralin – used for widespread, refractory plaques
Calcipotriene – as effective as topical glucocorticoids but slower onset; no long-term glucocorticoid adverse effects
Tazarotene – extended response; maintenance therapy

50
Q

Psoriasis systemic therapy

A

Used for patients with > 5% body surface area involvement
Methotrexate
- MOA: inhibits dihydrofolate reductase (folic acid analog)
- Used in combination with phototherapy or biological agents
- Effective for both skin lesions and arthritis

Acitretin

  • Systemic retinoic acid derivative
  • Not as effective as other systemic therapies

Cyclosporine

  • MOA: inhibits calcineurin, inhibits transcription of interleukin-1 and -2 receptors, blocks T-cell activation
  • ADRs: nephrotoxicity, hypertension, hepatotoxicity, gingival hyperplasia, and hirsutism
  • Used in extensive disease in patients who are unresponsive to other agents
51
Q

Psoriasis- Biologic Response Modifiers

A

Tumor necrosis factor inhibitors (etanercept, infliximab, adalimumab)

  • MOA: prevents TNF mediated immune responses
  • ADRs: risk of serious life-threatening infections (sepsis, pneumonia), exacerbation of congestive heart failure, and cause demyelinating disease in predisposed patients
  • What infectious disease must be ruled out before initiating therapy with TNF inhibitors?

TB

52
Q

Topical Corticosteroids

A

Immunosuppressive and anti-inflammatory
Local (topical & intralesional) or systemic (IM, IV, PO)
- Systemic therapy reserved for severe dermatological illness (allergic contact dermatitis to plants, life-threatening vesiculobullous dermatoses)
Corticosteroids are minimally absorbed following application to normal skin

53
Q

Regional variation of percutaneous corticosteroid absorption

A 
feet-- terrible
palm
forearm
scalp- getting better
forehead
genitalia- most
54
Q

Topical Corticosteroids

- groupings

A

Grouped into classes based on potency or approximate relative efficacy

Low to medium efficacy produce remission in disorders responsive to corticosteroids: seborrheic dermatitis, psoriasis of genitalia and face

High efficacy preparations useful in disorder less responsive to corticosteroids: psoriasis of palms and soles, sarcoidosis

ADRs: suppression of pituitary-adrenal axis
- Atrophy, steroid rosacea, steroid acne, allergic contact dermatitis

55
Q

lowest to highest efficacy of topical corticosteroids

A 
hydrocortisone
betamethasone valerate
hydrocortisone valerate
betamehasone dipropionate
Clobetasol propionate
56
Q

Keratolytic Agents

A

Keratolytic: peeling agent causing softening/dissolution or peeling of stratum corneum

Salicylic acid
Uses: acne, seborrheic dermatitis, psoriasis, hyperkeratosis (corns, plantar warts, calluses); in combination with antifungal sodium thiosulfate for tinea versicolor
Salicylate toxicity can occur (nausea, vomiting, dizziness, loss of hearing, tinnitus, lethargy, diarrhea, psychic disturbances)

57
Q

AntiPruritic Agents

A

Corticosteroids, local anesthetics
Topical therapy useful in localized pruritus
Systemic therapy generally used for generalized pruritus

Antihistamines
First generation H1-receptor antagonists
- Diphenhydramine, promethazine
- Some anticholinergic activity, sedating, useful in nocturnal pruritus

Second generation H1-receptor antagonists

  • Cetirizine, loratadine, desloratadine, fexofenadine
  • Do no cross blood-brain barrier, lack anticholinergic side effects, non-sedatin
58
Q

Trichogenic Agents

A

Trichogen: agent that promotes hair growth

Minoxidil
MOA: unknown
- Originally developed as an antihypertensive (PO dosing)
- Percutaneous absorption minimal but systemic effects on BP should be monitored in those with cardiac disease

Finasteride

  • MOA: competitive and selective inhibitor of steroid 5α-reductase; blocks the conversion of testosterone to dihydrotestosterone (DHT)
  • ADRs: decreased libido, ejaculation disorders, erectile dysfunction
  • Pregnant women should not handle drug

MSK II Exam I (16 decks)

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